Displaying publications 1 - 20 of 123 in total

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  1. Yusof MFH, Hashim SNM, Zahari W, Chandra H, Noordin KBAA, Kannan TP, et al.
    Appl Biochem Biotechnol, 2020 May;191(1):177-190.
    PMID: 32096060 DOI: 10.1007/s12010-020-03266-1
    Previously, it was reported that human amniotic membrane (AM) induced stem cells from human deciduous exfoliated teeth (SHED) endothelial-like-cell differentiation. This interesting effect of AM matrix on SHED demands further elucidation. Objective of this in vitro work was to study the effect of 24-h VEGF induced on SHED endothelial differentiation when seeded on acellular stromal side (SS) of AM matrix. Stemness of SHED was identified by flow cytometry. Cell attachment and morphological changes towards the matrix was observed by scanning electron microscopy. Protein expression of endothelial marker was examined by Western blot. The expression of stem cells and endothelial-specific gene markers of VEGF-induced SHED cultured on human AM was inspected via reverse transcriptase-polymerase chain reaction. Results showed SHED at both passages retain stemness property. Ang-1 protein was expressed in SHED. Cells treated with VEGF and cultured on AM transformed attached well to AM. VEGF-induced SHED expressed both stem cell and endothelial-specific markers throughout the treatments and timeline. Interestingly, prolonged VEGF treatment increased the expression of Cox-2 and VE-Cadherin genes in all treated groups when compared to SHED. It was concluded that the VEGF-induced SHED showed better expression of endothelial-specific markers when cultured on SS of AM, with prolonged VEGF treatment.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/pharmacology*
  2. Yong YK, Sulaiman N, Hakim MN, Lian GE, Zakaria ZA, Othman F, et al.
    Biomed Res Int, 2013;2013:463145.
    PMID: 24224164 DOI: 10.1155/2013/463145
    The aim of the present study was to evaluate the anti-inflammatory activities of aqueous extract of Bixa orellana (AEBO) leaves and its possible mechanisms in animal models. The anti-inflammatory activity of the extract was evaluated using serotonin-induced rat paw edema, increased peritoneal vascular permeability, and leukocyte infiltrations in an air-pouch model. Nitric oxide (NO), indicated by the sum of nitrites and nitrates, and vascular growth endothelial growth factor (VEGF) were measured in paw tissues of rats to determine their involvement in the regulation of increased permeability. Pretreatments with AEBO (50 and 150 mg kg⁻¹) prior to serotonin inductions resulted in maximum inhibitions of 56.2% of paw volume, 45.7% of Evans blue dye leakage in the peritoneal vascular permeability model, and 83.9% of leukocyte infiltration in the air-pouch model. 57.2% maximum inhibition of NO and 27% of VEGF formations in rats' paws were observed with AEBO at the dose of 150 mg kg⁻¹. Pharmacological screening of the extract showed significant (P < 0.05) anti-inflammatory activity, indicated by the suppressions of increased vascular permeability and leukocyte infiltration. The inhibitions of these inflammatory events are probably mediated via inhibition of NO and VEGF formation and release.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/metabolism
  3. Yong YK, Zakaria ZA, Kadir AA, Somchit MN, Ee Cheng Lian G, Ahmad Z
    PMID: 23410184 DOI: 10.1186/1472-6882-13-32
    Bixa orellana L. has been traditionally used in Central and South America to treat a number of ailments, including internal inflammation, and in other tropical countries like Malaysia as treatment for gastric ulcers and stomach discomfort. The current study aimed to determine the major chemical constituents of the aqueous extract of B. orellana (AEBO) and to evaluate the antihistamine activity of AEBO during acute inflammation induced in rats.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/metabolism
  4. Yong PH, New SY, Azzani M, Wu YS, Chia VV, Ng ZX
    Endocr Regul, 2023 Jan 01;58(1):26-39.
    PMID: 38345496 DOI: 10.2478/enr-2024-0004
    Hyperglycemia in diabetes mediates the release of angiogenic factors, oxidative stress, hypoxia, and inflammation, which in turn stimulate angiogenesis. Excessive angiogenesis can cause diabetic retinopathy, diabetic neuropathy, and diabetic nephropathy. All of these complications are debilitating, which may lead to an increased susceptibility to lower-limb amputations due to ulcerations and infections. In addition, microvascular alterations, segmental demyelination, and endoneurial microangiopathy may cause progressive deterioration ultimately leading to kidney failure and permanent blindness. Some medicinal plants have potent anti-angiogenic, antioxidant or anti-inflammatory properties that can ameliorate angiogenesis in diabetes. The purpose of this systematic review is to demonstrate the potential of medicinal plants in ameliorating the neovascularization activities in diabetes. Manuscripts were searched from PubMed, Science Direct, and Scopus databases, and Google Scholar was used for searching additional papers. From 1862 manuscripts searched, 1854 were excluded based on inclusion and exclusion criteria and 8 were included into this systematic review, whereas the required information was extracted and summarized. All identified medicinal plants decreased the high blood glucose levels in diabetes, except the aqueous extract of Lonicerae japonicae flos (FJL) and Vasant Kusumakar Ras. They also increased the reduced body weight in diabetes, except the aqueous extract of FL and total lignans from Fructus arctii. However, methanolic extract of Tinospora cordifolia and Vasant Kusumakar Ras were not tested for their ability to affect the body weight. Besides, all medicinal plants identified in this systematic review decreased the vascular endothelial growth factor (VEGF) protein expression and vasculature activity demonstrated by histopathological examination indicating promising anti-angiogenic properties. All medicinal plants identified in this systematic review have a potential to ameliorate neovascularization activities in diabetes by targeting the mechanistic pathways related to oxidative stress, inflammation, and angiogenesis.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  5. Yong MH, Amin A, Mushawiahti M, Bastion ML
    Med J Malaysia, 2015 Dec;70(6):358-60.
    PMID: 26988210
    We report a case of a middle-aged gentleman with recalcitrant macular oedema (RMO) secondary to ischaemic central retinal vein occlusion (CRVO). He was given six injections of intravitreal ranibizumab (anti-VEGF) monthly. However, his visual acuity (VA) deteriorated and the macular oedema worsened. He then received an intravitreal dexamethasone implant eight months post-CRVO. His VA and macular oedema improved dramatically and significantly at first follow-up and remained stable at six months after implant. This case can be a reference for those who treating recalcitrant macular oedema. It shows the effect of an intravitreal dexamathasone implant might have in a patient with RMO due to CRVO. The patient enjoyed improvement of vision, with clinical evidence of reduction in central macular thickness (CMT) and with no serious adverse events after a single injection up to six months post implant.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  6. Xian LJ, Chowdhury SR, Bin Saim A, Idrus RB
    Cytotherapy, 2015 Mar;17(3):293-300.
    PMID: 25456581 DOI: 10.1016/j.jcyt.2014.10.005
    Platelet-rich plasma (PRP) has been found to contain a high concentration of growth factors that are present during the process of healing. Studies conducted found that application of PRP accelerates wound healing. In this study, we characterized the skin cell suspension harvested using the co-isolation technique and evaluated the effects of PRP (10% and 20%, v/v) on co-cultured keratinocytes and fibroblasts in terms of wound healing.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/metabolism
  7. Wu LE, Meoli CC, Mangiafico SP, Fazakerley DJ, Cogger VC, Mohamad M, et al.
    Diabetes, 2014 Aug;63(8):2656-67.
    PMID: 24696450 DOI: 10.2337/db13-1665
    The vascular endothelial growth factor (VEGF) family of cytokines are important regulators of angiogenesis that have emerged as important targets for the treatment of obesity. While serum VEGF levels rise during obesity, recent studies using genetic models provide conflicting evidence as to whether VEGF prevents or accelerates metabolic dysfunction during obesity. In the current study, we sought to identify the effects of VEGF-A neutralization on parameters of glucose metabolism and insulin action in a dietary mouse model of obesity. Within only 72 h of administration of the VEGF-A-neutralizing monoclonal antibody B.20-4.1, we observed almost complete reversal of high-fat diet-induced insulin resistance principally due to improved insulin sensitivity in the liver and in adipose tissue. These effects were independent of changes in whole-body adiposity or insulin signaling. These findings show an important and unexpected role for VEGF in liver insulin resistance, opening up a potentially novel therapeutic avenue for obesity-related metabolic disease.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/genetics; Vascular Endothelial Growth Factor A/metabolism*
  8. Wong JG, Lai XJ, Sarafian RY, Wong HS, Smith JB
    Int Med Case Rep J, 2017;10:51-54.
    PMID: 28243154 DOI: 10.2147/IMCRJ.S107648
    We report a case of a Caucasian female who developed active polypoidal choroidal vasculopathy (PCV) at the edge of a stable choroidal nevus and was successfully treated with verteporfin photodynamic therapy. No active polyp was detectable on indocyanine green angiography 2 years after treatment, and good vision was maintained. Indocyanine green angiography is a useful investigation to diagnose PCV and may be underutilized. Unlike treatment of choroidal neovascularization secondary to choroidal nevus, management of PCV secondary to nevus may not require intravitreal anti-vascular endothelial growth factor therapy. Photodynamic monotherapy may be an effective treatment of secondary PCV.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  9. Weng-Yew W, Selvaduray KR, Ming CH, Nesaretnam K
    Nutr Cancer, 2009;61(3):367-73.
    PMID: 19373610 DOI: 10.1080/01635580802582736
    Previous studies have revealed that tocotrienol-rich fractions (TRF) from palm oil inhibit the proliferation and the growth of solid tumors. The anticancer activity of TRF is said to be caused by several mechanisms, one of which is antiangiogenesis. In this study, we looked at the antiangiogenic effects of TRF. In vitro investigations of the antiangiogenic activities of TRF, delta-tocotrienol (deltaT3), and alpha-tocopherol (alphaToc) were carried out in human umbilical vein endothelial cells (HUVEC). TRF and deltaT3 significantly inhibited cell proliferation from 4 microg/ml onward (P < 0.05). Cell migration was inhibited the most by deltaT3 at 12 microg/ml. Anti-angiogenic properties of TRF were carried out further in vivo using the chick embryo chorioallantoic membrane (CAM) assay and BALB/c mice model. TRF at 200 microg/ml reduced the vascular network on CAM. TRF treatment of 1 mg/mouse significantly reduced 4T1 tumor volume in BALB/c mice. TRF significantly reduced serum vascular endothelial growth factor (VEGF) level in BALB/c mice. In conclusion, this study showed that palm tocotrienols exhibit anti-angiogenic properties that may assist in tumor regression.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/antagonists & inhibitors; Vascular Endothelial Growth Factor A/blood
  10. Waziri PM, Abdullah R, Rosli R, Omar AR, Abdul AB, Kassim NK, et al.
    Asian Pac J Cancer Prev, 2018 Apr 25;19(4):917-922.
    PMID: 29693341
    Clausena excavata Burm f. is used by traditional healers to treat cancer patients in South East Asia. The use of the
    plant and its compounds is based on Asian folklore with little or no scientific evidence supporting the therapeutic efficacy
    The current study aimed to determine the effect of pure clausenidin isolated from C. excavata on caspase-8-induced cell
    death as well as angiogenesis in the HepG2 hepatocellular carcinoma cell line. Caspase-8 and extrinsic death receptor
    protein expression was determined using spectrophotometry and protein profile arrays, respectively. Ultrastructural
    analysis of clausenidin-treated cells was conducted using transmission electron microscopy. In addition, anti-angiogenic
    effects of clausenidin were investigated by Western blot analysis. Clausenidin significantly (p<0.05) increased the
    activity of caspase-8 and expression of protein components of the death inducing signaling complex (DISC) in HepG2
    cells. Ultrastructural analysis of the clausenidin-treated HepG2 cells revealed morphological abnormalities typical of
    apoptosis. Furthermore, clausenidin significantly (p<0.05) decreased the expression of vascular endothelial growth
    factor (VEGF). Therefore, clausenidin is a potential anti-angiogenic agent which may induce apoptosis of hepatocellular
    carcinoma cells.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/metabolism*
  11. Wang S, Yang J, Kuang X, Li H, Du H, Wu Y, et al.
    J Ethnopharmacol, 2024 May 23;326:117913.
    PMID: 38360380 DOI: 10.1016/j.jep.2024.117913
    ETHNOPHARMACOLOGICAL RELEVANCE: Kaempferia galanga Linn. is an aromatic medicinal herb with extensively applied in India, China, Malaysia and other South Asia countries for thousands of years. It has been mentioned to treat abdominal tumors. Ethyl cinnamate (EC), one of the main chemical constituents of the rhizome of K. galanga, exhibited nematocidal, sedative and vasorelaxant activities. However, its anti-angiogenic activity, and anti-tumor effect have not been investigated.

    AIM OF THE STUDY: To investigate the anti-angiogenic mechanism of EC and its anti-tumor effect by suppressing angiogenesis.

    MATERIALS AND METHODS: The in vitro anti-angiogenic effect was evaluated using HUVECs model induced by VEGF and zebrafish model in vivo. The influence of the EC on phosphorylation of VEGFR2 and its downstream signaling pathways were evaluated by western blotting assay. Molecule docking technology was conducted to explore the interaction between EC and VEGFR2. SPR assay was used for detecting the binding affinity between EC and VEGFR2. To further investigate the molecular mechanism of EC on anti-angiogenesis, VEGFR2 knockdown in HUVECs and examined the influence of the EC. Anti-tumor activity of EC was evaluated using colony formation assay and apoptosis assay. The inhibitory effect of EC on tumor growth was explored using HT29 colon cancer xenograft model.

    RESULTS: EC obviously inhibited proliferation, migration, invasion and tube formation of VEGF-induced HUVECs. EC also induced apoptosis of HUVECs. Moreover, it inhibited the development of vessel formation in zebrafish. Further investigations demonstrated that EC could suppress the phosphorylation of VEGFR2, and its downstream signaling pathways were altered in VEGF-induced HUVECs. EC formed a hydrogen bond to bind with the ATP binding site of the VEGFR2, and EC-VEGFR2 interaction was shown in SPR assay. The suppressive effect of EC on angiogenesis was abrogated after VEGFR2 knockdown in HUVECs. EC inhibited the colon cancer cells colony formation and induced apoptosis. In addition, EC suppressed tumor growth in colon cancer xenograft model, and no detectable hepatotoxicity and nephrotoxicity. In addition, it inhibited the phosphorylation of VEGFR2, and its downstream signal pathways in tumor.

    CONCLUSIONS: EC could inhibit tumor growth in colon cancer by suppressing angiogenesis via VEGFR2 signaling pathway, and suggested EC as a promising candidate for colon cancer treatment.

    Matched MeSH terms: Vascular Endothelial Growth Factor A/metabolism
  12. Vântu A, Ghertescu D, Fiscă C, Mărginean A, Hutanu A, Gheban D, et al.
    Malays J Pathol, 2019 Apr;41(1):25-32.
    PMID: 31025634
    INTRODUCTION: Experimental models are essential for clarifying the pathogenesis of atherosclerosis in the context of diabetes mellitus (DM). We aimed to evaluate the presence and the magnitude of several factors known to promote atherogenesis, and to assess the potential of a pro-atherogenic environment to stimulate the development of atherosclerotic lesions in a rat model of long-term type 1 DM.

    MATERIALS AND METHODS: Six control and five DM Wistar rats were evaluated. DM was induced at 11 weeks of age using streptozotocin (STZ; 60 mg/kg, intraperitoneal). Animals were monitored up to 38 weeks of age, when plasma glucose, lipid profile, and markers specific for systemic inflammation, endothelial dysfunction, and oxidative stress were measured. The amount of fat within the aortic wall was assessed semiquantitatively using Oil Red O staining.

    RESULTS: Diabetic rats presented significantly higher plasma glucose (p < 0.001), total cholesterol and triglycerides (both p = 0.02), high-sensitivity C-reactive protein (p = 0.01), and vascular endothelial growth factor (p = 0.04) levels, and significantly lower interleukin-10 (p = 0.04), superoxide dismutase (p < 0.01), and glutathione peroxidase (p = 0.01) levels than the control rats. Mild (grade 1) atherosclerotic lesions were observed in the aortic wall of 80% of the diabetic rats and in none of the control rats.

    CONCLUSIONS: This study presents a STZ-induced type 1 DM rat model with one of the longest follow-ups in the literature. In this model, long-term DM created a highly pro-atherogenic environment characterised by hyperglycemia, dyslipidemia, systemic inflammation, endothelial dysfunction, and oxidative stress that resulted in the development of early aortic atherosclerotic lesions.

    Matched MeSH terms: Vascular Endothelial Growth Factor A
  13. Umran NSS, Mohamed S, Lau SF, Mohd Ishak NI
    J Food Biochem, 2020 08;44(8):e13258.
    PMID: 32539198 DOI: 10.1111/jfbc.13258
    Diabetic cataract causes severe vision loss. This study evaluated the effects of hesperidin-standardized Citrus hystrix leaf flavonoids-rich extract (CLE) on diabetic-cataract development. Streptozotocin-induced diabetic rats were orally given 150 and 300 mg CLE/kg body-weight. These were compared with non-treated diabetic or healthy rats as controls, over 8 weeks. The CLE gradually attenuated fasting blood glucose (FBG), biomarkers for inflammation (Tumor necrosis factor alpha TNF-α; prostaglandin E2 PGE2); vascular permeability, (Vascular endothelial growth factor VEGF); and oxidative stress, (malondialdehyde MDA). The diabetic cataract was significantly mitigated by the 150 mg CLE/kg dose. Good correlations were found between cataract incidence with FBG (r2  = 0.90), serum PGE2 (r2  = 0.91), MDA (r2  = 0.99), VEGF (r2  = 0.71), but not with TNF-α levels (r2  = 0.49) suggesting the serum FBG, PGE2, MDA, and possibly the VEGF levels may help to predict the cataract risks. The CLE mitigated cataract probably by attenuating hyperglycaemia, inflammation, lens fluid influx, vascular leakage, lens osmotic-imbalance, and fibers over-hydration. PRACTICAL APPLICATIONS: The study shows the flavonoids-rich Citrus hystrix leaf consumption, effectively attenuated diabetes (fasting blood glucose) and mitigated diabetic cataract. It help reduce diabetes-related hyperglycaemia, oxidative stress, inflammation, and vascular leakage. The evidences were the CLE consumptions reduced the serum biomarkers tumor necrosis factor-alpha TNF-α; prostaglandin E2 PGE2, vascular endothelial growth factor (VEGF), and malondialdehyde (MDA). The C. hystrix leaf contains hesperidin, apiin, diosmin, saponarin, apigetrin, rutin and xanthotoxol, and other flavonoid glucosides. The study also showed good correlations between cataract incidence with fasting blood glucose FBG (r2  = 0.90), serum PGE2 (r2  = 0.91), and MDA (r2  = 0.99), and less closely with VEGF (r2  = 0.71) suggesting these serum biomarkers may help predict cataract risks. The CLE indicated cataract mitigation properties probably by attenuating FBG, inflammation, lens fluid influx, lens osmotic-imbalance, and fibers over-hydration.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  14. Umar MI, Asmawi MZ, Sadikun A, Majid AM, Al-Suede FS, Hassan LE, et al.
    Clinics (Sao Paulo), 2014 Feb;69(2):134-44.
    PMID: 24519205 DOI: 10.6061/clinics/2014(02)10
    The present study aimed to investigate the mechanisms underlying the anti-inflammatory and anti-angiogenic effects of ethyl-p-methoxycinnamate isolated from Kaempferia galanga.
    Matched MeSH terms: Vascular Endothelial Growth Factor A/analysis; Vascular Endothelial Growth Factor A/drug effects*
  15. Toulah FH, El-Aswad BEW, Harba NM, Naguib YM
    Trop Biomed, 2018 Dec 01;35(4):893-907.
    PMID: 33601839
    High-fat diet (HFD) can cause hyperlipidemia, fatty liver and cardiovascular disorders. Herein, we evaluated therapeutic effects and possible underlying mechanisms of actions of Schistosoma mansoni soluble egg antigen (SEA) against experimental HFD induced dyslipidemia, hepatic and cardiovascular pathology. Forty Swiss albino mice were divided into four groups (10 each); mice fed standard diet (SD), mice fed HFD, mice fed HFD for 8 weeks then infected by S. mansoni cercaria (HFD+I) and mice fed HFD for 8 weeks then treated with SEA (HFD+SEA), all mice were euthanized 16 weeks after starting the experiment. HFD+SEA mice showed significantly (p<0.001) reduced total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG), and significantly (p<0.05) increased high-density lipoprotein cholesterol (HDL-C) comparing to HFD mice with non-significant difference with HFD+I mice group. Doppler flowmetry showed significantly (p<0.01) lower arterial resistance and significantly (p<0.05) higher blood flow velocity in HFD+SEA and HFD+I mice groups than HFD mice. HFD+SEA mice revealed improving in liver and aortic pathology and these were better than HFD+I mice group. HFD+SEA and HFD+I mice groups had less myocardium lipid deposits, but still showing some congested blood vessels. HFD myocardium revealed strong CD34+ expression on immunohistochemistry study, while that of HFD+SEA showed weak and HFD+I mice had moderate expressions. HFD+SEA mice had significantly (p<0.01) lower serum IL-1β and vascular endothelial growth factor (VEGF) and significantly (p<0.001) higher serum transforming growth factor beta 1 (TGF-β1) and IL-10 than HFD mice with non-significant difference with HFD+I mice. In conclusion, SEA lowered serum lipids, improved aortic function, decreased liver and cardiovascular pathology in HFD mice, so, it is recommended to purify active molecules from SEA to develop anti-dyslipidemic treatment.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  16. Topchii II, Kirienko AN, Kirienko DA, Yakovtsova II, Gavriluk AA, Danyliuk SV, et al.
    Wiad Lek, 2019;72(7):1269-1273.
    PMID: 31398154
    OBJECTIVE: Introduction: Vascular endothelium function interruption has the main role among mechanisms of development and progression of chronic kidney disease. In numerous experimental and clinical studies, it was proved that activated vascular endothelium is a structural and functional unit that matches processes of inflammation with intravascular coagulation, fibrinolysis and haemorheological disorders. The aim: To identify special features of endothelium morphological structure in kidney vessels, coronary arteries and aorta during chronic kidney disease.

    PATIENTS AND METHODS: Materials and methods: Based on autopsy materials, we conducted a morphological study of patients (n = 20) aged 45 to 55 years who were observed in cardiac and neurological hospitals for 5-7 years. We removed kidney, heart and aorta samples from patients. For the study, a histological and immunohistochemical methods were used.

    RESULTS: Results and conclusions: Morphological study of vessels endothelium of kidneys, heart and aorta demonstrated that in the majority of observations intima underwentprofound pathological changes, manifested by different degrees of disorganization of endothelial lining and violations of structural and functional organization of the endotheliocytes, subendothelial layer, basal membrane. These pathological processes in all cases had similar features with the development of immune inflammation. Inflammatory infiltration was represented by macrophages, mast cells, plasma cells. Biological mediators of the presented cells can aggravate the damage to endothelial cells. Indirect signs of low ability to restore the structure of the vessel wall and endothelial lining may be a weak expression of the VEGF and bcl-2 vascular endothelial growth factor.

    Matched MeSH terms: Vascular Endothelial Growth Factor A
  17. Tekade RK, Tekade M, Kesharwani P
    Drug Discov Today, 2016 Jul 2.
    PMID: 27380716 DOI: 10.1016/j.drudis.2016.06.029
    The merger of nanotechnology and combination chemotherapy has shown notable promise in the therapy of resistant tumors. The latest scientific attention encompasses the engagement of anticancer drugs in combination with small interfering (si)RNAs, such as VEGF, XLAP, PGP, MRP-1, BCL-2 and cMyc, to name but a few. siRNAs have shown immense promise to knockout drug resistance genes as well as to recover the sensitivity of resistant tumors to anticancer therapy. The nanotechnology approach could also protect siRNA against RNAse degradation as well as prevent off-target effects. In this article, we discuss the approaches that have been used to deliver of siRNA in combination with chemotherapeutic drugs to treat resistant tumors. We also discuss the stipulations that must be considered in formulating a nanotechnology-assisted siRNA-drug cancer therapy.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  18. Tay KC, Tan LT, Chan CK, Hong SL, Chan KG, Yap WH, et al.
    Front Pharmacol, 2019;10:820.
    PMID: 31402861 DOI: 10.3389/fphar.2019.00820
    Cancer, a complex yet common disease, is caused by uncontrolled cell division and abnormal cell growth due to a variety of gene mutations. Seeking effective treatments for cancer is a major research focus, as the incidence of cancer is on the rise and drug resistance to existing anti-cancer drugs is major concern. Natural products have the potential to yield unique molecules and combinations of substances that may be effective against cancer with relatively low toxicity/better side effect profile compared to standard anticancer therapy. Drug discovery work with natural products has demonstrated that natural compounds display a wide range of biological activities correlating to anticancer effects. In this review, we discuss formononetin (C16H12O4), which originates mainly from red clovers and the Chinese herb Astragalus membranaceus. The compound comes from a class of 7-hydroisoflavones with a substitution of methoxy group at position 4. Formononetin elicits antitumorigenic properties in vitro and in vivo by modulating numerous signaling pathways to induce cell apoptosis (by intrinsic pathway involving Bax, Bcl-2, and caspase-3 proteins) and cell cycle arrest (by regulating mediators like cyclin A, cyclin B1, and cyclin D1), suppress cell proliferation [by signal transducer and activator of transcription (STAT) activation, phosphatidylinositol 3-kinase/protein kinase-B (PI3K/AKT), and mitogen-activated protein kinase (MAPK) signaling pathway], and inhibit cell invasion [by regulating growth factors vascular endothelial growth factor (VEGF) and Fibroblast growth factor 2 (FGF2), and matrix metalloproteinase (MMP)-2 and MMP-9 proteins]. Co-treatment with other chemotherapy drugs such as bortezomib, LY2940002, U0126, sunitinib, epirubicin, doxorubicin, temozolomide, and metformin enhances the anticancer potential of both formononetin and the respective drugs through synergistic effect. Compiling the evidence thus far highlights the potential of formononetin to be a promising candidate for chemoprevention and chemotherapy.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  19. Tang YQ, Jaganath I, Manikam R, Sekaran SD
    PMID: 23690850 DOI: 10.1155/2013/609581
    Phyllanthus is a traditional medicinal plant that has been found to have antihepatitis, antibacterial, and anticancer properties. The present studies were to investigate the in vitro molecular mechanisms of anticancer effects of Phyllanthus (P. amarus, P. niruri, P. urinaria, and P. watsonii) plant extracts in human prostate adenocarcinoma. The cancer ten-pathway reporter array was performed and revealed that the expression of six pathway reporters were significantly decreased (Wnt, NFκB, Myc/Max, hypoxia, MAPK/ERK, and MAPK/JNK) in PC-3 cells after treatment with Phyllanthus extracts. Western blot was conducted and identified several signalling molecules that were affected in the signalling pathways including pan-Ras, c-Raf, RSK, Elk1, c-Jun, JNK1/2, p38 MAPK, c-myc, DSH, β-catenin, Akt, HIF-1α, GSK3β, NFκB p50 and p52, Bcl-2, Bax, and VEGF, in treated PC-3 cells. A proteomics-based approach, 2D gel electrophoresis, was performed, and mass spectrometry (MS/MS) results revealed that there were 72 differentially expressed proteins identified in treated PC-3 cells and were involved in tumour cell adhesion, apoptosis, glycogenesis and glycolysis, metastasis, angiogenesis, and protein synthesis and energy metabolism. Overall, these findings suggest that Phyllanthus can interfere with multiple signalling cascades involved in tumorigenesis and be used as a potential therapeutic candidate for treatment of cancer.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
  20. Tan BL, Norhaizan ME, Chan LC
    Pharmaceutics, 2018 Oct 23;10(4).
    PMID: 30360519 DOI: 10.3390/pharmaceutics10040198
    Magnetic iron oxide nanoparticles are among the most useful metal nanoparticles in biomedical applications. A previous study had confirmed that phytic acid-chitosan-iron oxide nanocomposite (Phy-CS-MNP) exhibited antiproliferative activity towards human colorectal cancer (HT-29) cells. Hence, in this work, we explored the in vitro cytotoxicity activity and mechanistic action of Phy-CS-MNP nanocomposite in modulating gene and protein expression profiles in HT-29 cell lines. Cell cycle arrest and apoptosis were evaluated by NovoCyte Flow Cytometer. The mRNA changes (cyclin-dependent kinase 4 (Cdk4), vascular endothelial growth factor A (VEGFA), c-Jun N-terminal kinase 1 (JNK1), inducible nitric oxide synthase (iNOS), and matrix metallopeptidase 9 (MMP9)) and protein expression (nuclear factor-kappa B (NF-κB) and cytochrome c) were assessed by quantitative real-time polymerase chain reaction (PCR) and western blotting, respectively. The data from our study demonstrated that treatment with Phy-CS-MNP nanocomposite triggered apoptosis and G₀/G₁ cell cycle arrest. The transcriptional activity of JNK1 and iNOS was upregulated after treatment with 90 μg/mL Phy-CS-MNP nanocomposite. Our results suggested that Phy-CS-MNP nanocomposite induced apoptosis and cell cycle arrest via an intrinsic mitochondrial pathway through modulation of Bax and Bcl-2 and the release of cytochrome c from the mitochondria into the cytosol.
    Matched MeSH terms: Vascular Endothelial Growth Factor A
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